Modulation of the sensitivity of nicotinic receptors in autonomic ganglia

Akasu, Takashi; Tokimasa, Takayuki

doi:10.1007/978-3-0348-9138-7_19

Cited by 8 publications

(6 citation statements)

References 22 publications

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“…Conversely, Colomo et al (1968) showed that 5-hydroxytryptamine (5HT) antagonizes the action of acetylcholine (ACh) at the neuromuscular junction of the adult frog. This result was later confirmed by Magazanik et al (1976) as reported by Akasu and Tokimasa (1989), but the mechanism of 5HT action has not been elucidated. Inhibition of nAChR function by 5HT was found also in peripheral neurons, where it was ascribed to competitive antagonism (for review see Akasu and Tokimasa, 1989).…”

Section: Introductionsupporting

confidence: 90%

“…This result was later confirmed by Magazanik et al (1976) as reported by Akasu and Tokimasa (1989), but the mechanism of 5HT action has not been elucidated. Inhibition of nAChR function by 5HT was found also in peripheral neurons, where it was ascribed to competitive antagonism (for review see Akasu and Tokimasa, 1989). More recently, it has been demonstrated that 5HT binds to G-proteincoupled 5HTR (i.e., 5HT,R, 5HT,R, and 5HT,R), and to a ligand-gated ion channel 5HTR (i.e., 5HT,R) (Julius, 1991).…”

Section: Introductionsupporting

confidence: 90%

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Blockage of nicotinic acetylcholine receptors by 5‐hydroxytryptamine

Grassi¹,

Polenzani

Mileo³

et al. 1993

J of Neuroscience Research

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The action of 5-hydroxytryptamine (5HT) on nicotinic acetylcholine receptor (nAChR) channels was investigated in mouse myotubes, human cloned TE671/RD cells, and Xenopus laevis oocytes. The decay of the ACh-activated whole-cell currents was reversibly accelerated in the presence of 5HT (10(-5) to 10(-3) M), in a dose-dependent manner. 5HT also reduced the size and accelerated the decay of currents elicited by ACh in Xenopus oocytes injected with mRNA extracted from C2 myotubes or Torpedo electroplaques, or oocytes injected with cloned mouse muscle AChR subunit mRNAs. The effect of 5HT was promptly reversed after washout, or by depolarizing the oocyte beyond -10 mV. In patch-clamp recordings from myotubes, bath-application of 5HT did not exert an indirect influence on the ACh-activated channels within the patch membrane. In contrast, when the patch membrane was exposed to 5HT (10(-6) M), ACh unit responses appeared as bursts of short pulses. It is concluded that the regulation of ACh responses by 5HT results from a fast noncompetitive blocking action of nAChR-channels. These results show that ligand-gated channels, activated by their specific neurotransmitter, may be regulated by a different neurotransmitter through a direct action on the receptor molecule.

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Section: Introductionsupporting

confidence: 90%

Section: Introductionsupporting

confidence: 90%

Blockage of nicotinic acetylcholine receptors by 5‐hydroxytryptamine

Grassi¹,

Polenzani

Mileo³

et al. 1993

J of Neuroscience Research

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“…High-affinity uptake and storage of 5-HT have been shown in bovine adrenal chromaffin cells (Slotkin and Kirschner, 1971). 5-HT has been previously shown to reduce nicotinic responses of bullfrog sympathetic neurons, frog motor endplate, and rabbit parasympathetic ganglia (Akasu and Koketsu, 1986;Akasu and Tokimasa, 1989). In a recent article (Schmid and Vijayaraghavan, 1992), we have shown that nicotinic responses in ciliary ganglion neurons, which are thought to express similar AChR gene products as chromaffin cells (Boulter et al, 1986;Boyd et al, 1988), are similarly modulated by 5-HT.…”

mentioning

confidence: 76%

“…These intriguing findings that adrenergic and noradrenergic agents block nicotinic responses, but that the endogenous catecholamines tested have no effect, motivated the present study. 5-HT presents a likely candidate to mediate feedback inhibition because it is a biogenic amine shown to be present in chromaffin cells from many species (Brownfield et al, 1985;Delarue et al, 1988;Kong et al, 1989;Garcia-Arraras and Martinez, 1990) and also because it has been shown to inhibit nicotinic responses in other systems (Colomo et al, 1968;Akasu and Koketsu, 1986;Akasu and Tokimasa, 1989;Schmid and Vijayaraghavan, 1992).…”

Section: Discussionmentioning

confidence: 99%

Serotonin Modulates Nicotinic Responses of Adrenal Chromaffin Cells

Vijayaraghavan

Schmid

Mapp

1993

Journal of Neurochemistry

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5-Hydroxytryptamine (5-HT) specifically and reversibly inhibits nicotine-induced currents and catecholamine release in bovine adrenal chromaffin cells in culture. Pharmacological analysis indicates that the inhibition is not mediated by known 5-HT receptor subtypes. The inhibition is noncompetitive over a range of nicotine concentrations between 1 and 100 microM. Preincubation with either 5-HT or substance P significantly protects the response from nicotine-induced desensitization. It is concluded that 5-HT inhibits nicotinic acetylcholine receptors on bovine adrenal chromaffin cells, probably by binding to a noncompetitive site on the receptor itself. Because both blood and the chromaffin cells contain 5-HT, the inhibition provides an opportunity for negative control of catecholamine secretion from the adrenals.

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“…Although AcChoRs are potently activated or blocked by specific cholinergic agents, it is becoming increasingly evident that serotonin ], a widely distributed neurotransmitter, is also a strong blocker of both muscle and neuronal AcChoRs (20)(21)(22)(23)(24). The present experiments were aimed at finding out if the effects of 5HT required receptors of a particular subunit composition.…”

mentioning

confidence: 98%

Serotonergic modulation of muscle acetylcholine receptors of different subunit composition.

Garcı́a-Colunga

Miledi

1996

Proc. Natl. Acad. Sci. U.S.A.

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Modulation of muscle acetylcholine (AcCho) receptors (AcChoRs) by serotonin The structure-function relationship of muscle AcChoRs has been studied by altering their glycosylation, subunit structure, and subunit composition. These changes were found to alter the levels of receptor expression (4), receptor assembly and membrane incorporation (5-10), agonist sensitivity (11-13), and channel gating or desensitization (14)(15)(16)(17)(18)(19)

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Modulation of the sensitivity of nicotinic receptors in autonomic ganglia

Cited by 8 publications

References 22 publications

Blockage of nicotinic acetylcholine receptors by 5‐hydroxytryptamine

Blockage of nicotinic acetylcholine receptors by 5‐hydroxytryptamine

Serotonin Modulates Nicotinic Responses of Adrenal Chromaffin Cells

Serotonergic modulation of muscle acetylcholine receptors of different subunit composition.

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